Redox Regulation in Inflammation and Disease—3rd Edition

A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: 20 October 2025 | Viewed by 1589

Special Issue Editors


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Guest Editor
Department of Otorhinolaryngology, University Medicine Essen, Essen, Germany
Interests: redox regulation; signal transduction; TRX family proteins; (neuro-) inflammation; cell communication; tumor–stroma crosstalk; neutrophil biology; translational immunology
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Guest Editor Assistant
Cell Biology and Neuroscience “De Robertis” Institute (IBCN), Medical Faculty, University of Buenos Aires, Buenos Aires, Argentina
Interests: neurodegenerative diseases; axonal transport; redox regulation; mitochondrial homeostasis; TRX family proteins

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Guest Editor Assistant
Department of Dermatology and Allergology, Philipps-Universität Marburg, Marburg, Germany
Interests: autoimmunity; animal models; autoimmune bullous diseases; redox regulation; translational immunology

Special Issue Information

Dear Colleagues,

We differentiate between oxidative eu- and distress, recognizing the role of various factors such as i) the regulated enzymatic production and decay of specific reactive oxygen species (ROS), ii) their role as second messengers, and iii) the presence of regulatory thiol switches and their function in redox-mediated signaling.

Specific reactive species, including hydrogen peroxide, hydrogen sulfide, and nitric oxide, are essential for physiological processes including metabolism and signal transduction, as well as cell proliferation, differentiation, and death. Redox regulation of (membrane) proteins, enzymes, and transcription factors such as NFκB is crucial for the chemotaxis and activation of immune cells, the production and release of immune mediators, and cell communication within distinct physiological and pathological microenvironmental niches. Interestingly, extracellular redox proteins, low-molecular-weight thiols, and thiol switches can also affect signal transduction and cell communication.

Changes in the expression, protein levels, or distribution of specific redox proteins can be assessed using histological techniques. These changes have been associated with many disorders linked to ischemia and inflammation and more specifically to distinct subpopulations of immune cells.  Redox changes can be analyzed in body fluids and isolated immune cell populations without using invasive and expensive techniques, maintaining their potential for developing new preventive and diagnostic tools and innovative treatments.

For this Special Issue, we invite researchers to provide original research articles that report results combining the topics of redox regulation, inflammatory signaling, and translational immunology. We encourage studies that highlight the role of specific reactive species, redox proteins, and/or thiol switches. Additionally, we welcome clinical studies demonstrating significant changes in the levels or activities of i) redox proteins, ii) low-molecular-weight thiols, and/or iii) altered redox states of proteins in diseases linked to inflammation or neuroinflammation. Review articles discussing the current state of the art are also welcome.

Yours faithfully,

Dr. Eva-Maria Hanschmann
Guest Editor

Dr. Mariana Ines Holubiec
Dr. Christoph Hudemann
Guest Editor Assistants

Manuscript Submission Information

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Keywords

  • redox signaling
  • reactive oxygen and nitrogen species
  • inflammation
  • signal transduction
  • thiol switches
  • regulation of immune cells
  • translational immunology

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Published Papers (2 papers)

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Review

29 pages, 2797 KiB  
Review
Allosteric Disulfide Bridges in Integrins: The Molecular Switches of Redox Regulation of Integrin-Mediated Cell Functions
by Johannes A. Eble
Antioxidants 2025, 14(8), 1005; https://doi.org/10.3390/antiox14081005 (registering DOI) - 16 Aug 2025
Abstract
Almost every cell of a multicellular organism is in contact with the extracellular matrix (ECM), which provides the shape and mechanic stability of tissue, organs and the entire body. At the molecular level, cells contact the ECM via integrins. Integrins are transmembrane cell [...] Read more.
Almost every cell of a multicellular organism is in contact with the extracellular matrix (ECM), which provides the shape and mechanic stability of tissue, organs and the entire body. At the molecular level, cells contact the ECM via integrins. Integrins are transmembrane cell adhesion molecules that connect the ECM to the cytoskeleton, which they bind with their extracellular and intracellular domains. Cysteine residues are abundant in both integrin subunits α and β. If pairwise oxidized into disulfide bridges, they stabilize the folding and molecular structure of the integrin. However, despite the oxidative environment of the extracellular space, not all pairs of cysteines in the extracellular integrin domains are permanently engaged in disulfide bridges. Rather, the reversible and temporary linkage of cystine bridges of these cysteine pairs by oxidation or their reductive cleavage can cause major conformational changes within the integrin, thereby changing ligand binding affinity and altering cellular functions such as adhesion and migration. During recent years, several oxidoreductases and thiol isomerases have been characterized which target such allosteric disulfide bridges. This outlines much better, albeit not comprehensively, the role that such thiol switches play in the redox regulation of integrins. The platelet integrin αIIbβ3 is the best examined example so far. Mostly referring to this integrin, this review will provide insights into the thiol switch-based redox regulation of integrins and the known effects of their allosteric disulfide bridges on conformational changes and cell functions, as well as on the machinery of redox-modifying enzymes that contribute to the redox regulation of cell contacts with the ECM. Full article
(This article belongs to the Special Issue Redox Regulation in Inflammation and Disease—3rd Edition)
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31 pages, 1370 KiB  
Review
Redox Imbalance in Inflammation: The Interplay of Oxidative and Reductive Stress
by Francesco Bellanti, Anna Rita Daniela Coda, Maria Incoronata Trecca, Aurelio Lo Buglio, Gaetano Serviddio and Gianluigi Vendemiale
Antioxidants 2025, 14(6), 656; https://doi.org/10.3390/antiox14060656 - 29 May 2025
Cited by 3 | Viewed by 1118
Abstract
Redox imbalance plays a pivotal role in the regulation of inflammation, influencing both the onset and progression of various inflammatory conditions. While the pro-inflammatory role of oxidative stress (OS) is well established, the impact of reductive stress (RS)—a condition marked by excessive reducing [...] Read more.
Redox imbalance plays a pivotal role in the regulation of inflammation, influencing both the onset and progression of various inflammatory conditions. While the pro-inflammatory role of oxidative stress (OS) is well established, the impact of reductive stress (RS)—a condition marked by excessive reducing equivalents such as NADH, NADPH, and reduced glutathione (GSH)—remains underappreciated. This review offers a novel integrative perspective by analyzing how OS and RS act not merely in opposition, but as interconnected modulators of immune function. We explore the mechanisms through which OS activates inflammatory pathways, and how RS, when sustained, can paradoxically impair immune defense, alter redox-sensitive signaling, and contribute to disease progression. Emphasis is placed on the dynamic interplay between these redox extremes and their combined contribution to the pathogenesis of chronic inflammatory diseases, including autoimmune, cardiovascular, and neuroinflammatory disorders. Additionally, we evaluate therapeutic strategies that target redox homeostasis, arguing for a shift from antioxidant-centric treatments to approaches that consider the bidirectional nature of redox dysregulation. This framework may inform the development of more precise interventions for inflammation-related diseases. Full article
(This article belongs to the Special Issue Redox Regulation in Inflammation and Disease—3rd Edition)
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